Funds are requested to support travel and conference fees for scientists to the 13th bi-annual Gordon research conference on Mutagenesis, at Bates College, Lewiston, Maine, July 28-August 2, 2002. The selected speakers are experts in the field of mutagenesis, and the Conference will provide the opportunity to discuss their latest results and ideas. The meeting will serve as a forum for extensive interactions among all attending scientists through the Discussion Sessions and the Poster Presentations. Selected poster presenters, generally students and young scientists, will be given the opportunity to introduce their research results for discussion in short presentations (five minutes with overheads but not powerpoint or slides). The Conference is usually heavily oversubscribed with attendance limited to 135 persons. Participants are selected from universities, government research laboratories, regulatory agencies, research institutes, and industrial laboratories worldwide. Specific efforts are made and special consideration is given to encouraging attendance from minority groups, women, graduate students, and persons with disabilities. The 2002 Conference will extend our understanding of the mechanisms by which mutations occur and the strategies employed by organisms to control and modulate mutagenesis. Nine sessions will include topics on nucleotide and base-excision repair, standard and new error-prone DNA polymerases, mismatch repair and genetic instability, recombination and double-strand break repair, structural, kinetic and theoretical determinants of DNA polymerase, mismatch repair and genetic instability, recombination and double-strand break repair, structural, kinetic and theoretical determinants of DNA polymerase fidelity, somatic hypermutation of immunoglobulins and mutagenesis and genetic instability in evolution and human disease. The Conference will examine mutagenesis from biochemical, molecular, structural, physical chemical, genetic and theoretical viewpoints. The field of mutagenesis is critical to human health because spontaneous and exogeneously induced mutations can initiate and facilitate the progression of a multitude of human diseases, particularly cancer and neurodegenerative diseases, while accumulation of endogenous oxidative lesions is implicated in aging.